W3 - Appetite regulation & Energy Balance Flashcards
Describe early theory of appetite control?
- Food intake mechanism of temperature regulation (1948)
- There is a relationship between serum amino acid concentration & appetite fluctuations (1955)
- Glucostatic mechanism of regulation of food intake - diabetics(1953)
- Fat stores play a role on the hypothalamic control of food intake in the rat - allows them to know how much energy(leptin) the body has in reserve (1953)
What was obesity determined as in 1960’s?
What is a circulating factor that regulates body weight? found be Douglas Coleman & Jeffrey Friedman
Describe the experiment used to find the gene for obesity:
- In the 1960’s obesity was rare, thought was due to a behavioural issue
- Douglas Coleman & Jeffrey Friedman identified a damaged hypothalamus influenced the feeling of fullness and hunger, changing eating behaviour accordingly
- Wanted to find the genetic basis of obesity, so joined different pairs of mice to see if there was similarities
- 2 mutant mouse models (ob/ob & db/db) were identified displaying hyperphagia(excessive eating) and obesity
- Defined as ob/ob and db/db – having genetic mutations on different chromosomes
- Parabiosis experiments used to test the hypothesis that a circulating factor may be mediating the obese phenotype in these animals
What are the two parts of neuro-humoral regulation of appetite?
- Set-point theory/principle
- Neuro-humoral model
What is meant by a negative energy balance?
Explain the Set point principle of Leptin to regulate adiposity
What type of feedback is this?
Negative energy balance = Correction response by body, much more robust than high energy balance(putting weight on)
–> Body goes into survival, body defends against negative energy balance
-Leptin (in adipose tissue) is monitored in the hypothalamus
- When Leptin is low –> Brain (switch off processes that are high in energy expenditure)
- stops reproductive processes
- Activating SNS
- Negative feedback
Explain the dual intervention point model:
- Middle Zone
- Upper and Lower Boundaries
Why do people put weight on faster/slower?
- Middle zone is were nothing much happens to the body
- Upper and lower boundaries of physiological regulation (passive control in-between boundaries)
- Lower boundary imposed by starvation and infection pressure
- Upper boundary imposed by predation
- Weak upper boundary
- Determined by genetics
- People that put on weight quite easily have a wider middle zone before the body elicits responses
- Lower(narrower) zone has evolved due to survival pressures, higher zone evolved because of privation(running away from danger)
Describe the neuro-humoral appetite control system (homeostatic)
How is Ghrelin involved?
- Periphery ↔ brain
- Tonic signals
- Episodic signals
- Circulation
- Vagus nerve
- Hypothalamus (arcuate nucleus
Peptides from the gut/intestine travel to the brain to tell us to stop eating –> satiety
- Ghrelin levels increase signalling with meal initiation and hunger
What drive us to consume the amount of food we do per day?
- Most signals work in a negative feedback –> satiety peptides
- Lean mass and metabolic rate is the biggest factor that regulates appetite
- Higher metabolic rates in bigger people cause them to eat more per day
What hormone is largely impacted when there is an energy deficit?
After weight loss causes people to be hungrier and have higher ghrelin levels once people have lost weight
What are the two hormones which signal a long-term energy balance?
Leptin and Insulin
Circulating leptin correlates positively with body fat
- Explain the northern & western blot
- What does Goldthloglucose cause?
Northern blot - leptin gene expression in SCAT is elevated in rodents rendered obese by chemical, HFD and age
- Goldthloglucose damages adipose tissue leptin, expression of leptin goes up as animals become obese
Western blot – circulating levels of leptin decline with energy restriction & weight loss
- Energy balance effect the production of leptin in adipose tissue either when making animals learner or more obese
What is myogenic obesity?
What is polygenic obesity?
How do genetics influence the risk of obesity?
Why is a Leptin injection not always the answer?
- Monogenic obesity - single gene that is linked to the risk of obesity –> causes person to be obese through childhood as the brain thinks you are starving
- Polygenic obesity - multiple genes that are linked to obesity
- Genetics can increase the risk of becoming obese
- Someone not producing enough leptin proteins can be 2x their body weight as the brain is receiving signals that they are satiated (solved through exogenous leptin injection)
- Leptin is really high in obese people there is no response to it unless it drops
- When leptin drops obesity cannot be solved through a leptin injection
Describe the post-prandial responses in the satiety cascade
sensory
cognitive
post-ingestive
post-absorptive
What effect would infusing insulin have on the body?
What can increase the effect of injecting insulin?
Infusing insulin into the body can cause changes in body weight
- Causes animals to eat less
- Shows interlinking of acute system of hormones with long term system of hormones
- Insulin injected with CCK causes a larger effect than insulin alone
Describe the hormones and their roles in episodic(acute) regulation
Ghrelin - correlates to hunger(stimulates feeding via arcuate nucleus neurones)
Leptin - correlates to satiety
- Circular system is undergone around 3 times a day
What role does insulin play pre-prandial?
Insulin buffers the state of hunger as the body prepares to eat food
- Cephalic phase of digestion –> Initiated by the sight and smell of food
